Obesity is a common comorbidity in asthma. The ?obese asthma? phenotype exhibits worse control and response to steroids and more severe symptoms. The mechanisms leading to such a phenotype include low-grade inflammation and the mechanistic influence of obesity on the lungs. However, data on inflammatory profile and lung function in animal obesity models are conflicting and limited mainly to mice.

The aim of the study was to assess if diet-induced obesity worsens respiratory status in rats.

Twelve juvenile male Brown Norway rats (n=6/group) were given either high-fat high-sugar (HFHC) or chow diet (C) for 12 weeks. Rats had free access to water and feed during the study. Rats? pulmonary parameters were assessed by double-chamber plethysmography (DCP) once a week from the start of the study. After 12 weeks of respective diets, animals were decapitated. Serum, lungs, and visceral fat were collected for metabolic profile assessment in serum (glucose, insulin, leptin, triglycerides, cholesterol, NEFA), lung histology, and Il-6 and Tnf-? mRNA levels in lungs and visceral fat by qPCR.
The HFHC rats had higher levels of glucose (p=0.0009), cholesterol (p=0.0013), and NEFA (p=0.0057) compared to C. However, we did not observe any changes in lung histology (bronchi muscle layer thickness, airway mucus amount) between HFHC and C rats. Lung function parameters: tidal volume (TV) and pulmonary ventilation did not differ in HFHC rats compared to C (p=0.39 and p=0.66, respectively).

Data obtained during the study suggest that diet-induced obesity does not affect pulmonary status in juvenile rats.

National Science Centre OPUS grant 2019/35/B/NZ5/02906.